Vibrio cholerae (V. cholerae) is a non-invasive enteropathogen of the small bowel that does not penetrate the mucosal surface. Local SIgA mediated immunity at the mucosal surface is therefore implicated as a protective mechanism. Pathogenic V. cholerae 01 elaborate a protein enterotoxin (also known as cholera enterotoxin, or choleragen, or cholera toxin) which is responsible for induction of copious secretion by the intestine resulting in watery diarrhea, the clinical consequence of cholera infection. Cholera diarrhea can be extraordinarily severe and result in loss of so much body water and salts that dehydration, acidosis, shock, and death ensue without prompt therapy.
The cholera vaccines that have been developed can be broadly divided into two categories; those aiming to stimulate antitoxic immunity and those intending to induce antibacterial immunity. Experiments with animal models support a protective role for either or both antitoxic and antibacterial immunity. It has been suggested that when both types of immunity work in unison, there is a synergistic effect. [Holmgren, J. et al. J. Infect. Dis. 136 Suppl., S105-S1122 (1977); Peterson, J. W. Infect. Immun. 26, 594 (1979); Resnick, I. G. et al. Infect. Immun. 13, 375 (1980); Svennerholm, A.-M. et al. Infect. Immun. 13, 735 (1976)]. However, it appears that protective immunity in humans can be conferred without such synergistic effect, that is by either antitoxic immunity or antibacterial immunity [Eubanks, E. R. et al. Infect. Immun. 15, 533 (1977); Fujita, K. et al. J. Infect. Dis. 125, 647 (1972); Holmgren, J., J. Infect. Dis., supra; Lange, S. et al. Acta Path. Microbiol. Scand Sect. C. 86, 145 (1978); Peterson, J. W., supra (1979); Pierce, N. F. et al. Infect. Immun. 37, 687 (1982); Pierce, N. F. et al. Infect. Immun. 21, 185 (1978); Pierce, N. F. et al. J. Infect. Dis. 135, 888 (1977); Resnick, I. G. et al., supra; Svennerholm, A.-M. et al, supra].